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Cholecystectomy-related gut microbiota dysbiosis promotes colorectal tumorigenesis by interrupting FXR/β-catenin interaction

ABSTRACT: Cholecystectomy-related gut microbiota dysbiosis promotes colorectal tumorigenesis

PROVIDER: PRJEB66177 | ENA |

REPOSITORIES: ENA

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human gut metagenome

Project description:Cholecystectomy-related gut microbiota dysbiosis promotes colorectal tumorigenesis

| PRJNA1056543 | ENA

Cholecystectomy-related gut microbiota dysbiosis exacerbates colorectal tumorigenesis.

Project description: Not available

| S-EPMC12357946 | biostudies-literature

Multiomic analysis reveals a role of Fusobacterium periodonticum in colorectal tumorigenesis by decanoic acid promoting neutrophil chemotaxis

Project description:Gut microbiota dysbiosis and immune dysregulation are closely linked to colorectal cancer development. Identifying mechanistic connections among specific microbial species, metabolites, and immune responses may reveal novel insights into its pathogenesis. Here, employing metagenomic, metabolomic, and single-cell transcriptomic analyses across clinical cohorts, we identify Fusobacterium periodonticum as significantly enriched in colorectal cancer patients and strongly correlated with elevated decanoic acid levels, and further reveal tissue-specific neutrophil enrichment in colorectal cancer. Cellular experiments demonstrate that decanoic acid induces neutrophil late apoptosis/necrosis and enhances chemotaxis through a pertussis toxin-sensitive G-protein-dependent mechanism, while upregulating genes associated with leukocyte migration and tumorigenesis. Mouse models further confirm that F. periodonticum colonization increases dysplasia and decanoic acid levels, and that decanoic acid intervention promotes tumor progression through neutrophil infiltration and immune modulation. Our study reveals an important role of F. periodonticum in colorectal tumorigenesis via decanoic acid-medicated neutrophil chemotaxis, providing new insights into colorectal cancer pathogenesis

2026-05-20 | MTBLS14505 | MetaboLights

SLC26A9 promotes colorectal tumorigenesis by modulating Wnt/β-catenin signaling.

Project description: Not available

| S-EPMC10925040 | biostudies-literature

IRF3 prevents colorectal tumorigenesis via inhibiting the nuclear translocation of β-catenin

Project description:Occurrence of Colorectal cancer（CRC）is relevant with gut microbiota. However, role of IRF3, a key signaling mediator in innate immune sensing, has been barely investigated in CRC. Here, we unexpectedly found that the IRF3 deficient mice are hyper-susceptible to the development of intestinal tumor in AOM/DSS and Apcmin/+ models. Genetic ablation of IRF3 profoundly promotes the proliferation of intestinal epithelial cells via aberrantly activating Wnt signaling. Mechanically, IRF3 in resting state robustly associates with the active β-catenin in the cytoplasm, thus preventing its nuclear translocation and cell proliferation, which can be relieved upon microbe-induced activation of IRF3. In accordance, the survival of CRC is clinically correlated with the expression level of IRF3. Therefore, our study identifies IRF3 as a negative regulator of the Wnt/β-catenin pathway and a potential prognosis marker for Wnt-related tumorigenesis, and describes an intriguing link between gut microbiota and CRC via the IRF3-β-catenin axis.

2020-09-16 | GSE155777 | GEO

FXR suppresses colorectal cancer by inhibiting the Wnt/β-catenin pathway via activation of TLE3.

Project description: Not available

| S-EPMC10308151 | biostudies-literature

IRF3 prevents colorectal tumorigenesis via inhibiting the nuclear translocation of β-catenin

Project description:IRF3 prevents colorectal tumorigenesis via inhibiting the nuclear translocation of β-catenin

| PRJNA655560 | ENA

Ceramide-mediated gut dysbiosis enhances cholesterol esterification and promotes colorectal tumorigenesis in mice.

Project description: Not available

| S-EPMC8855812 | biostudies-literature

IRF3 prevents colorectal tumorigenesis via inhibiting the nuclear translocation of β-catenin.

Project description: Not available

| S-EPMC7666182 | biostudies-literature

DNA methylation profiles of mouse sperm in response to antibiotic-induced gut microbiota dysbiosis using whole-genome bisulfite sequencing

Project description:DNA methylation profile of mouse sperm from conventionally-raised mice and gut dysbiosis experienced mice were characterized using whole-genome bisulfite sequencing. Genome-wide DNA methylation changes between control and dysbiotic male�s sperm were highly comparable, with no change in DNAme globally or at genomic features, only 21 differentially methylated regions (DMR) were identified, which did not overlap known regulatory elements. Epididymal sperm samples were harvested from 11 weeks old inbred male mice that were experiencing gut microbiota dysbiosis for 6-week (antibiotics treated, n=5), or drink sterilized water (control, n=5).

2023-11-13 | E-MTAB-10033 | biostudies-arrayexpress

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